For months, it seemed that the more we learned about COVID-19, the worse the news was. It apparently wasn’t enough for the coronavirus to be unpredictable in whether infection carried mild or lethal consequences because recovery can carry its own challenges.
By now, you’ve likely heard of the “long haul” patients who experience severe symptoms weeks after the virus is no longer present in their bodies. And if that wasn’t enough, reports of permanent and potentially life-threatening brain issues prompted even greater concern about the long-term effects of the virus.
However, it seems we finally have the potential for some encouraging news as evidence is mounting to suggest a landmark theory into how the virus works may actually equip us to understand it.
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Soon after the COVID-19 outbreak was officially declared a pandemic, researchers in two different countries noticed the way it seemed to affect a peptide called bradykinin.
As The Scientist magazine reported , Daniel Jacobson at Tennessee’s Oak Ridge National Laboratory and Frank van de Veerdonk at the Radboud University Medical Center in The Netherlands both noticed that the bradykinin receptors in infected bodies were more active than usual.
Under normal circumstances, bradykinin helps to regulate the body’s blood pressure and balance its fluids.
But when the body produces too much bradykinin, it dilates the blood vessels so much that they start to leak.
As The Scientist reported , this phenomenon is known as a “bradykinin storm” and van de Veerdonk suspected that it may be responsible for the fluid build-up in the lungs and the widespread inflammation often observed in COVID-19 patients.
As a release from the Oak Ridge National Laboratory outlined , Jacobson noticed that common coronavirus symptoms also matched a known bradykinin-related disease called hereditary angioedema.
But of the two men, only Jacobson had access to the lab’s Summit supercomputer, which is one of the most powerful computers in the world.
According to the Oak Ridge National Laboratory , the Summit is theoretically capable of running 200 quadrillion calculations per second and Jacobson’s team needed it to analyze the gene expressions of nine COVID-19 patients to 17,000 samples from uninfected people.
This would normally take months with standard desktop computers, but Summit was able to analyze the data in a week.
And the supercomputer’s results confirmed that the bodies of COVID-19 patients not only overproduce bradykinin but also inhibit the production of enzymes that break it down. This gives us the conditions for leaking blood vessels that researchers suspected.
As Jacobson put it, “If that happens in the lung, that’s not good. Immune cells that are normally contained in the blood vessels flood into the surrounding infected tissue, causing inflammation.”
To make matters worse, COVID-19 was found to similarly overproduce hyaluronic acid, a gooey substance in the body’s connective tissues that forms a hydogel by trapping up to 1,000 times its weight in water.
And this one-two punch effect seems to go a long way towards explaining why severe COVID-19 cases can be lethal even when the patients are on ventilators.
As Jacobson said , “When the lungs end up with an excess of hyaluronic acid in them, it’s like trying to breathe through Jell-O. It reaches a point where regardless of how much oxygen you pump in, it doesn’t matter, because the alveoli in the lungs are filled with this hydrogel.
“With this excess of hyaluronic acid, any water leaking out of the blood vessels due to bradykinin will soak up this structure and the lungs become like a water balloon.”
The potential good news to emerge from these findings are that at least 10 medications already exist to treat bradykinin-related conditions.
However, the Oak Ridge National Laboratory cautioned that it will take large-scale clinical trials to determine whether or not these medications are effective at treating extreme COVID-19 symptoms.
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According to The Scientist , trials involving at least a couple of these drugs are already underway.
As Jacobson said, “If we can block this pathogenesis in severe patients, we can keep the human response from going overboard and give their immune system time to fight off the virus so they can recover.”
